A mechanistic study published in the Proceedings of the National Academy of Sciences has identified how physical activity protects muscle health during aging. Researchers found that exercise suppresses DEAF1, a transcription factor that becomes overactive with age and disrupts the cellular balance between protein synthesis and autophagy—the process by which cells remove damaged components.
In young muscle, mammalian target of rapamycin complex 1 (mTORC1) maintains equilibrium between building new proteins and clearing cellular waste. However, in aging muscle, DEAF1 overactivity drives excessive mTORC1 signaling while impairing autophagy, accelerating muscle loss and weakness. Animal model studies confirmed that exercise-induced DEAF1 suppression restores this youthful balance, suggesting the transcription factor represents a viable therapeutic target for age-related sarcopenia.
These findings reinforce exercise as the most evidence-based intervention for maintaining muscle strength and mass in older adults.
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